insulin resistance, type 1 and type 2 diabetes, and...

EditorialInsulin Resistance, Type 1 and Type 2 Diabetes, and RelatedComplications 2017

Joseph Fomusi Ndisang,1 Alfredo Vannacci,2 and Sharad Rastogi3

1Department of Physiology, University of Saskatchewan College of Medicine, 107 Wiggins Road, Saskatoon, SK, Canada S7N 5E52Department of Neurosciences, Psychology, Drug Research and Child Health Section of Pharmacology and Toxicology,University of Florence, Viale Pieraccini 6, 50139 Florence, Italy3The Medical Affairs Company, Cardiovascular, Troy, MI 48085, USA

Correspondence should be addressed to Joseph Fomusi Ndisang; [email protected]

Received 13 August 2017; Accepted 13 August 2017; Published 15 November 2017

Copyright © 2017 Joseph Fomusi Ndisang et al. This is an open access article distributed under the Creative CommonsAttribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the originalwork is properly cited.

The global escalation of obesity and diabetes in developedand developing nations poses a great health challenge.Obesity is one of the major causes of type 2 diabetes. Type1 diabetes is primarily due to the autoimmune-mediateddestruction of pancreatic beta cell leading to insulin defi-ciency [1–3]. This is usually accompanied by alterations inlipid metabolism, enhanced hyperglycemia-mediated oxida-tive stress, endothelial cell dysfunction, and apoptosis [1–3].Similarly, in type 2 diabetes, increased glucotoxicity, lipotoxi-city, endoplasmic reticulum-induced stress, and apoptosislead to the progressive loss of beta cells [1–5]. While type 1diabetes is characterized by the presence of beta cell auto-antibodies, a combination of peripheral insulin resistanceand dysfunctional insulin secretion by pancreatic beta cellsis implicated in the pathogenesis of type 2 diabetes [1–3].However, both forms of diabetes are associated by a widevariety of complications such as cardiomyopathy, nephropa-thy, and neuropathy. Although insulin resistance has tradi-tionally been associated with type 2 diabetes, mountingevidence indicates that the incidence of insulin resistance intype 1 diabetes is increasing [6]; therefore, novel mechanisticapproaches deciphering insulin resistance are needed. Manypathophysiological factors are implicated in insulin resistance[5, 7]. Although the exact natures of these factors are notcompletely understood, it is widely accepted that oxidativestress, inflammation, and genetic, habitual, environmental,and other epigenetic factors play a significant role.

In the past two decades, significant strides have beenmade in elucidating important mechanisms associated withinsulin resistance, overt diabetes, and related cardiometabolicdiseases. However, more intense research is still needed fora more comprehensive understanding of the pathophysio-logical profile of insulin resistance in diabetes, especiallyin situations where diabetes is comorbid with other chronicdiseases. Therefore, this special issue is a collection ofresearch and review papers that address a broad range ofmechanisms associated with insulin resistance, type 1 diabe-tes, type 2 diabetes, and related cardiometabolic complica-tions. A common pathophysiological destructive force intype 1 and type 2 diabetes is the high levels of advancedglycation end products generated by hyperglycaemia [1–3].To unveil further insights on advanced glycation endproducts, T. Okura et al. wrote an article on the putativepathophysiological role of advanced glycation end productson deregulation of insulin signalling in type2 diabetes.To further expatiate on dysfunctional insulin signalling,F. De C. Cartolano et al. investigated the impact of insulinresistance on lipid metabolism at preclinical level andfound that insulin resistance and diabetes are powerfulpredictors of quantitative and qualitative features of lipopro-tein dysfunction and are directly associated with increasedatherogenic risk.

Dyslipidaemia, obesity, and visceral adiposity are com-mon risk factors for insulin resistance, type 2 diabetes, and

HindawiJournal of Diabetes ResearchVolume 2017, Article ID 1478294, 3 pageshttps://doi.org/10.1155/2017/1478294

https://doi.org/10.1155/2017/1478294

cardiovascular complications [8, 9]. To shed more insight onthis theme, C. Fujii et al. investigated the relationshipsbetween the composition of free fatty acids and metabolicparameters and found that serum linoleic acid is negativelycorrelated with the accumulation of visceral fat and insulinresistance. On the other hand, Y. Long et al. investigatedthe effects of overexpressing gamma-glutamyltransferaseon insulin sensitivity and found the short-term overex-pression of liver-specific gamma-glutamyltransferase ame-liorates insulin sensitivity. Although liver disease commonlyoccurs in diabetes, other organ complications includingcardiomyopathy, neuropathy, and nephropathy are highlydocumented [1, 2, 4, 5]. To underscore the role of the kidneyin diabetes and hypertension, U. Kampmann et al. gave theirinsights on effects of renal denervation on insulin sensitivityin nondiabetic patients with treatment for resistant hyper-tension in an article featuring in this special issue. On theother hand, to give further insight on diabetic neuropathy,L. Luo et al. wrote an article underscoring gene profiles ofneurotrophin-mitogen-activated protein kinase (MAPK)signalling in patients with diabetic peripheral neuropathy.

Besides obesity, another important habitual factor thataffects the development of insulin resistance and type2 diabe-tes is sedentary lifestyle. Moreover, sedentary lifestyle is oneof the modifiable risk factors of type 2 diabetes and the valueof exercise to improve insulin signalling and glucose metab-olism cannot be overemphasized [10]. Accordingly, in aresearch article, C. J. Gaffney et al. investigated how acuterestoration of normoglycemia affected energy metabolismduring exercise in nonobese patients with type 2 diabetes.The authors reported that insulin-induced normoglycemiaincreased blood glucose during subsequent exercise withoutaltering overall substrate utilization. Similarly, in anotherarticle on exercise, S. Benedini et al. underscored the benefitsof sports in enhancing insulin sensitivity and glucose metab-olism and suggested a putative role of the exercise-inducedmyokine and irisin in the beneficial effects of exercise onglucose metabolism. Irisin is a protein produced in themuscles during exercise [11]. Generally, small incrementsof irisin levels in the blood trigger a parallel incrementin energy expenditure in mammals with no changes inmovement or food intake [11].

Besides exercise, weight-loss surgeries are referred to asbariatric surgery is adopted to reduce health risks associatedwith obesity [12]. Among the different types of bariatricsurgeries is Roux-en-Y gastric bypass surgery [12]. In arelated article featuring in this special issue, X. Zhao et al.explored the impact of Roux-en-Y gastric bypass surgery oncardiovascular risk in diabetic patient comorbid with obesity.The authors showed that the Roux-en-Y gastric bypasssurgery is an effective strategy to mitigate cardiovascular riskin diabetic patients with comorbid of obesity. In addition tosurgery, another emerging therapeutic pathway featuring inthis special issue is a review article by J. A. David et al. wherethe authors highlighted the role of the nuclear-factor-E2-related-factor-2 (Nrf2)/kelchlike ECH-associated-protein-1(Keap1)/antioxidant response element (ARE) pathway as atarget for prevention, prognosis, and treatment of type 2diabetes. The Nrf2/Keap1/ARE has been well documented

for its cytoprotective effects, with potential therapeuticapplications [13].

Collectively, the articles featuring in this special issuecover a wide breadth of topics of great interest and wouldbenefit a wide audience.

Joseph Fomusi NdisangAlfredo VannacciSharad Rastogi

References

[1] M. Mishra and J. F. Ndisang, “A critical and comprehensiveinsight on heme oxygenase and related products includingcarbon monoxide, bilirubin, biliverdin and ferritin in type-1and type-2 diabetes,” Current Pharmaceutical Design, vol. 20,no. 9, pp. 1370–1391, 2014.

[2] J. F. Ndisang and A. Jadhav, “Hemin therapy improveskidney function in male streptozotocin-induced diabeticrats: role of the heme oxygenase/atrial natriuretic peptide/adiponectin axis,” Endocrinology, vol. 155, no. 1, pp. 215–229, 2014.

[3] M. C. Petersen, D. F. Vatner, and G. I. Shulman, “Regula-tion of hepatic glucose metabolism in health and disease,”Nature Reviews Endocrinology, vol. 13, no. 10, pp. 572–587, 2017.

[4] J. F. Ndisang, A. Jadhav, and M. Mishra, “The heme oxy-genase system suppresses perirenal visceral adiposity, abatesrenal inflammation and ameliorates diabetic nephropathy inZucker diabetic fatty rats,” PLoS One, vol. 9, no. 1, articlee87936, 2014.

[5] P. Hossain, B. Kawar, and M. El Nahas, “Obesity and dia-betes in the developing world—a growing challenge,” TheNew England Journal of Medicine, vol. 356, no. 3, pp. 213–215, 2007.

[6] M. Vladu, D. Clenciu, I. C. Efrem et al., “Insulin resistanceand chronic kidney disease in patients with type 1 diabetesmellitus,” Journal of Nutrition and Metabolism, vol. 2017,Article ID 6425359, 5 pages, 2017.

[7] J. F. Ndisang and A. Jadhav, “Heme arginate therapyenhanced adiponectin and atrial natriuretic peptide, butabated endothelin-1 with attenuation of kidney histopatholog-ical lesions in mineralocorticoid-induced hypertension,” TheJournal of Pharmacology and Experimental Therapeutics,vol. 334, no. 1, pp. 87–98, 2010.

[8] L. Duvnjak and M. Duvnjak, “The metabolic syndrome: anongoing story,” Journal of Physiology and Pharmacology,vol. 60, Supplement 7, pp. 19–24, 2009.

[9] J. F. Ndisang and M. Mishra, “The heme oxygenase systemselectively suppresses the proinflammatory macrophage m1phenotype and potentiates insulin signaling in spontaneouslyhypertensive rats,” American Journal of Hypertension, vol. 26,no. 9, pp. 1123–1131, 2013.

[10] B. K. Pedersen, “Anti-inflammatory effects of exercise: role indiabetes and cardiovascular disease,” European Journal ofClinical Investigation, vol. 47, no. 8, pp. 600–611, 2017.

[11] P. Bostrom, J. Wu, M. P. Jedrychowski et al., “A PGC1-α-dependent myokine that drives brown-fat-like developmentof white fat and thermogenesis,” Nature, vol. 481, no. 7382,pp. 463–468, 2012.

2 Journal of Diabetes Research

[12] G. K. Dimitriadis, M. S. Randeva, and A. D. Miras, “Potentialhormone mechanisms of bariatric surgery,” Current ObesityReports, vol. 6, no. 3, pp. 253–265, 2017.

[13] Z. Zhang, S. Zhou, X. Jiang et al., “The role of the Nrf2/Keap1 pathway in obesity and metabolic syndrome,”Reviews in Endocrine & Metabolic Disorders, vol. 16, no. 1,pp. 35–45, 2015.

3Journal of Diabetes Research

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